Disturbances of the redox state of the beta cell may be involved in the pathogenesis of beta cell viability and anomalies in insulin release observed in diabetes. The chemical diabetogenic agents streptozotocin and alloxan appear to cause irreversible changes in the redox state of the beta cell which lead to cell damage and resultant diabetes. On the other hand, very small changes in the redox state of the beta cell by sulfhydryl agents appear to modify insulin release. The present study intends to further define the mechanisms through which redox changes occur in the beta cell and the effect of these changes on cell viability and insulin release by the following investigations. Firstly, to assess the effects of toxic doses of streptozotocin and alloxan on beta cell viability by changes in the reduced to oxidized glutathione ratio, changes in the ratio of reduced to oxidized pyridine nucleotides, on the production of free radicals, and on the effect of these agents on the activity of the hexose monophosphate shunt. Secondly, to assess the effect of small changes in the beta cell redox state on insulin release brought about by low concentrations of oxidant or sulfhydryl agents. Thirdly, to characterize the acute metabolic events following M. strain EMC virus-induced diabetes in mice, and to assess whether this virus induces changes in the redox state of cells.